ArticleScientific reports2021
A gain-of-function NLRP3 3'-UTR polymorphism causes miR-146a-mediated suppression of NLRP3 expression and confers protection against sepsis progression.
Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 18 citations in OpenAlex.
- The NLRP3 inflammasome in physiological and dysfunctional host response in human sepsis and critical illness: a narrative review.Critical care (London, England) · 2026Review
- Inflammasome Gene Polymorphisms (NLRP3 and NLRC4) and Vitamin D Status in Patients with Multiple Sclerosis.International journal of molecular sciences · 2026Article
- Functional significance of NLRP3 polymorphisms in mild cognitive impairment.BMC geriatrics · 2026Article
- Association of NLRP3 Inflammasome rs10754558 Polymorphism with Type 2 Diabetes Mellitus and Its Complications: Clinical and Bioinformatics Study.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Article
- Review
- Concurrent genotyping and expression of NLRP3 inflammasome in pityriasis versicolor patient's skin lesions.Archives of dermatological research · 2024Article
- Review
- The NLRP3 inflammasome rs35829419 C>A polymorphism is associated with type 2 diabetes mellitus in Saudi Arabia.Saudi medical journal · 2023Article
- Review
- Molecular mechanisms and functions of pyroptosis in sepsis and sepsis-associated organ dysfunction.Frontiers in cellular and infection microbiology · 2022Review
- The Impact of NLRP3 Activation on Hematopoietic Stem Cell Transplantation.International journal of molecular sciences · 2021Review
- Bacteria and Sepsis: Microbiome to the Rescue?Journal of clinical medicine · 2021Review
- Investigation of Association of Complement 5 Genetic Polymorphisms with Sepsis and Sepsis-Induced Inflammatory Responses.Journal of inflammation research · 2021Article
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Nucleotide-binding domain and leucine-rich repeat (LRR)-containing family protein 3 (NLRP3) regulated the maturation of inflammation-related cytokines by forming NLRP3 inflammasome, which plays pivotal roles in sepsis pathogenesis. In this study, we evaluated the genetic association of NLRP3 polymorphisms with sepsis (640 patients and 769 controls) and characterized the impact of NLRP3 polymorphisms on NLRP3 expression and inflammatory responses. No significant differences were observed in genotype/allelic frequencies of NLRP3 29940G>C between sepsis cases and controls. The G allele was significantly overrepresented in patients with septic shock than those in sepsis subgroup, and the GC/GG genetypes were related to the 28-day mortality of sepsis. Lipopolysaccharide challenge to peripheral blood mononuclear cells showed a significant suppression of NLRP3 mRNA expression and release of IL-1β and TNF-α in CC compared with the GC/GG genotype category. Functional experiments with luciferase reporter vectors containing the NLRP3 3'-UTR with the 29940 G-to-C variation in HUVECs and THP-1 cells showed a potential suppressive effect of miR-146a on NLRP3 transcription in the presence of the C allele. Taken together, these results demonstrated that the 29940 G-to-C mutation within the NLRP3 3'-UTR was a gain-of-function alteration that caused the suppression of NLRP3 expression and downstream inflammatory cytokine production via binding with miR-146a, which ultimately protected patients against susceptibility to sepsis progression and poor clinical outcome.
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